Dr. R. R. Humphrey of Indiana University has reported the discovery of a gene, designated c for cardiac nonfunction, in the Mexican axolotl, Ambystoma mexicanum. The gene is recessive and lethal. The effect of homozygosity for gene c is the absence of initiation of a heart beat, even though the heart apparently develops in a normal fashion at first; later the heart becomes distended and thin-walled and the animal becomes edematous. The affected salamanders survive for 14 to 21 days after the time when the heart would normally have started to beat. I propose to study this birth defect in the following ways: (1) Cardiac cells from normal ad affected embryos will be placed in tissue culture so alterations in the chemical environment can be studied. Mutant cardiac cells will be used as a tool to study the action of the normal allele of gene c. (2) Since Humphrey has shown that the cardiac nonfunction defect can be corrected by transplantation of the heart primordia from mutant embryos into normal hosts, a biochemical study will be done in which normal heart primordia will be fractionated and the corrective substance isolated. The tissue culture technique of mutant heart cells will be utilized to bioassay the chemical preparations obtained from normal embryonic hearts.